Whitaker A N, Bunce I, Nicoll P, Dowling S V
Am J Pathol. 1973 Jul;72(1):1-12.
Because of the importance of the renin-angiotensin system in renal homeostatic mechanisms, the effect of angiotensin administration upon disseminated intravascular coagulation has been studied in rabbits. An infusion of angiotensin II (0.1 mug/kg/min for 2 hours) produced neither histologic abnormalities in the kidneys nor an elevation of creatinine. After an infusion of thrombin (2.0 units/kg/min for 2 hours) only 3 of 10 rabbits, when sacrified 24 hours later, showed histologic lesions comprised of occasional fibrin thrombi and foci of tubular necrosis. Creatinine levels did not rise. In contrast, the combination of angiotensin and thrombin resulted in renal lesions in 12 of 14 animals. Four had frank cortical necrosis, while combinations of tubular necrosis, glomerular thrombosis and segmental glomerular infarction occurred in the others, together with elevated creatinine levels. Blockade of alpha-adrenoreceptors with phenoxybenzamine in 12 animals did not prevent either these histologic changes or creatinine elevation, showing that the effect of angiotensin was independent of alpha-adrenoreceptor stimulation. The synergistic interaction between angiotensin and disseminated intravascular coagulation was not explained by differences in the consumption of plasma fibrinogen but apparently was due to localization of fibrin thrombi within glomerular capillaries by the vasomotor actions of angiotensin, as has previously been shown to occur with alpha-adrenoreceptor simulation. Such a mechanism might contribute to renal glomerular deposition of fibrin in acute ischemic renal failure.
由于肾素 - 血管紧张素系统在肾脏稳态机制中的重要性，已在兔子身上研究了给予血管紧张素对弥散性血管内凝血的影响。输注血管紧张素 II（0.1微克/千克/分钟，持续2小时）既未导致肾脏出现组织学异常，也未使肌酐升高。在输注凝血酶（2.0单位/千克/分钟，持续2小时）后，24小时后处死的10只兔子中只有3只出现了组织学病变，包括偶尔的纤维蛋白血栓和肾小管坏死灶。肌酐水平未升高。相比之下，血管紧张素和凝血酶联合使用导致14只动物中的12只出现肾脏病变。4只出现明显的皮质坏死，其他动物则出现肾小管坏死、肾小球血栓形成和节段性肾小球梗死的组合，同时肌酐水平升高。在12只动物中用酚苄明阻断α - 肾上腺素能受体并不能预防这些组织学变化或肌酐升高，表明血管紧张素的作用独立于α - 肾上腺素能受体刺激。血管紧张素与弥散性血管内凝血之间的协同相互作用不能用血浆纤维蛋白原消耗的差异来解释，显然是由于血管紧张素的血管舒缩作用使纤维蛋白血栓定位于肾小球毛细血管内，正如先前已证明α - 肾上腺素能受体刺激时会发生的那样。这种机制可能导致急性缺血性肾衰竭时纤维蛋白在肾小球沉积。
